#4051 FGF-23 IN CHRONIC KIDNEY DISEASE: CORRELATION WITH BONE AND CARDIOVASCULAR PARAMETERS – A PRELIMINARY STUDY

Abstract

Abstract Background and Aims The FGF-23/Klotho ratio increases from early stages of chronic kidney disease (CKD) in parallel with kidney function declined. In some cases, serum FGF-23 levels increase is unbalanced, causing organ damage and increasing cardiovascular risk. The aim of our study was to evaluate the intact FGF-23 (iFGF-23) levels in a cohort of CKD patients and to establish its correlation with cardiovascular and bone mineral metabolism parameters. Method A prospective observational study in 59 adult normophosphatemic patients with CKD stage 2-4, was performed. Clinical and analytical variables (serum calcium, phosporus, intact parathyroid hormone (iPTH), iFGF-23, calcidiol and calcitriol) were evaluated. Basal transthoracic echocardiogram, bone densitometry (Lunar prodigy, GE iDXA), software trabecular bone score (TBS), iNsight clinical data analyzer and carotid Doppler ultrasound were performed. We excluded patients with background of primary hyperparathyroidism, hepatorenal polycystic disease, kidney transplant, tumoral nephrectomy, active neoplasm, tubulopathies or treatment with active vitamin D or calcimimetics. For statistical analysis, we use SPSS software (T Student, Xi2, Fisher test, ANOVA test, U-Mann Whitney test and correlations of Pearson and Spearman) Results Mean age was 62,7±10,5 years, 82,5% were men; 17,7% have CKD stage 2, 28,8% stage 3a, 42,3% stage 3b and 9,6% stage 4. The main CKD etiology was vascular (25%) and diabetes (22%). Previous cardiovascular disease was observed in 11% (ischemic heart disease 6,3%, cerebrovascular disease 3,2% and descompensated heart failure with hospitalization 1,6%). Mean iFGF-23 levels in CKD stage 2 were 80,4±38 ng/l (38-170, median 71 ng/l), in CKD stage 3a 95,5±39,7 ng/l (46-178,9 ng/l, median 85,5 ng/l), in CKD stage 3b 118,8±55,06 (35,5-285 ng/l, median 124,6 ng/l) and in stage 4 134,8±50,9 ng/l (65,25-216,5 ng/l, median 136,1 ng/l). We found correlation between iFGF-23 levels and glomerular filtration rate (Rho:-0,390, p: 0,003), as well as with CKD stages (ANOVA test, p: 0,057). We performed 48 carotid doppler ultrasound and observed mild carotid atheromatosis in 58,7%, mainly bilateral, and intima-media thickness >0,9 mm in 7,9%. In patients with atheromatosis, 38,9% showed iFGF-23 levels in second tertil and 36% in the third. We observed left ventricular hypertrophy (LVH) in 46% of patients, mostly mild degree. In bone densitometry, we found mean femoral neck T-Score of -1±1,1 and lumbar spine T-Score of -0,07±1,5, mean mineral bone density (DMO) in femoral neck of 0,89±0,25 g/cm2 and 1,17±0,20 g/cm2 in lumbar spine. Only 40% of patients had normal TBS score. We found correlation between serum iFGF-23 levels and phosphorus tubular reabsorption (r:-0,396, p: 0,002), calcidiol (Rho: 0,264, p:0,047), calcitriol (r: -0,412, p:0,002), iPTH (Rho: 0,296, p:0,025), lumbar T-Score (r: -0,320 p:0,022), lumbar DMO (r:-0,267, p:0,049) and TBS (r: -0,396, p:0,005). Conclusion We confirm an association between a glomerular filtration rate decline and an increase in serum iFGF-23 levels. The inverse correlation observed between iFGF-23 serum levels and lumbar T-Score, lumbar DMO and trabecular microarchitecture suggests a negative effect of iFGF-23 in bone mineralization.